In diseases characterized by chronic immune responses, unprimed T and B lymphocytes are under excessive replication pressure, resulting in age-inappropriate telomeric shortening, the accumulation of DNA damage, and ultimately, increased rates of apoptosis in these lymphocytes. Increased attrition of these naïve lymphocytes imposes lymphopenia-induced proliferation, leading to premature immunosenescence and an autoimmune-biased lymphocyte repertoire. For example, in Rheumatoid Arthritis (RA), an autoimmune disease characterized by synovial inflammation and destruction of the joint architecture, naïve CD4+ T cells accumulate DNA double strand breaks and demonstrate an increased susceptibility to apoptosis, resulting in an accumulation of pro-inflammatory T-effector cell populations and loss of tolerance to neo-antigens. Restoration of DNA repair mechanisms in these naïve lymphocytes, either by promoting DNA double strand break repair (DSBR) or by preventing apoptosis until the cell's DSBR machinery can repair DNA damage, thus emerges as an important therapeutic approach in these diseases. The present invention addresses these issues.